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An autoimmune response to herniated nucleus pulposus has been proposed to constitute a pathophysiologic mechanism for inducing sciatica based on the fact that nucleus pulposus under normal conditions is excluded from the development of immunological tolerance. The manifestation of an autoimmune response comprises different steps starting with antigen capture, continuing with activation of T helper (T(H)) cells and ending with production of autoantibodies. Activated T(H) cells differentiate into either T(H)1 cells, predominately producing proinflammatory cytokines such as interferon gamma (IFNgamma) or a T(H)2 subset mainly producing anti-inflammatory cytokines such as interleukin-4 (IL-4). The aim of the present study was to examine if exposure of autologous nucleus pulposus (NP) to the immune system for 3 weeks is potent enough to prime T(H) cells to differentiate into T(H)2 cells. The study was performed in a pig model allowing the exposure of NP to the immune system. To assess the polarization of T(H) cells the intracellular production of IFNgamma and IL-4 was measured in T cells by using flow cytometry. The revealed predominant production of IL-4 together with low production of IFNgamma in T cells after NP exposure to the immune system indicates that nucleus pulposus may prime T(H) cells to develop into IL-4-producing T(H)2 cells after being exposed to the immune system, for example, in association with disc herniation.

A well-controlled animal model is presented for the study of neuromuscular injury induced by a pneumatic tourniquet. This model comprises a curved tourniquet surrounded by a stiff exterior shell, both of which were specifically designed to fit the conical and oblong shape of the rabbit hindlimb. Computed tomographic imaging was used to assess transverse tissue displacement induced by tourniquet compression. The curved tourniquet/shell configuration occluded the distal arterial blood flow to the extremity at a significantly lower cuff inflation pressure than a straight tourniquet of equal width. The magnitude and distribution of tissue pressures in the subcutaneous and deep tissues beneath the tourniquet were similar to those recorded in previous human cadaver studies of tourniquet compression. This animal model will facilitate the quantitation and analysis of tissue injury induced beneath and distal to a pneumatic tourniquet. Such data can help define the critical pressure and time limits for the safe use of pneumatic tourniquets in extremity surgery.

Peripheral nerves are often mechanically stretched in association with trauma to extremities, resulting in varying degrees of impairment of nerve function. However, little is known about the biomechanical properties of peripheral nerves and limits of stretching that the nerve may undergo before structural changes occur. Also, the injury pattern of nerves under stretching is poorly understood. In the present study, fresh rabbit tibial nerves (n = 18) were harvested. Nine nerves were stretched to failure in an INSTRON materials testing machine at a rate of 1 cm/min (strain rate of 0.5%/s). Load-deformation and stress-strain curves were determined. Histological examination by light microscopy of the stretched nerves as well as six normal control nerves and three clamped nonstretched control nerves was performed. The results show that the rabbit tibial nerves have an in situ strain of 11.0 +/- 1.5% and exhibit a nonlinear stress-strain relationship. After 20% strain, the curve becomes linear up to failure. The ultimate strain and tensile strength of the nerves were 38.5 +/- 2.0% and 11.7 +/- 0.7 MPa, respectively. At failure, the load dropped suddenly, but the specimens remained grossly intact. Histological analysis of the stretched nerves showed multiple ruptures of perineurial sheaths when compared to controls.

Compression injuries of spinal nerve roots are very common. However, the basic pathophysiology of these conditions is not fully understood. In this study a model is presented for experimental graded compression of the nerve roots of the pig cauda equina, including a technique for vital microscopic studies on the microcirculation flow of the intrinsic vessels of the nerve roots during compression. With this model critical pressure levels for compression-induced occlusion of the arterioles, capillaries, and venules of the intrinsic vasculature of the nerve roots were determined. The study showed that the average minimum pressure in the inflated balloon required to stop the flow in the arterioles was 127 mm Hg (SD = 18, n = 11), in the capillaries 40 mm Hg (SD = 6, n = 12), and in the venules 30 mm Hg (SD = 10, n = 12). The average mean arterial pressure (MAP) was 150 mm Hg (SD = 14, n = 12). There was a statistically significant correlation (p greater than 0.001) between the MAP and the pressure required to stop the flow in the arterioles (r = 0.83, n = 14), but no correlation between MAP and capillary (r = 0.09 NS, n = 20) or venular (r = -0.28 NS, n = 34) occlusion pressure. After the nerve roots had been compressed at 50 or 200 mm Hg for 10 min or 2 h, the recirculation started immediately. There was a hyperemia during the first 10 min, with a dilatation of the vessels, particularly the venules. In nerve roots exposed to compression for 2 h at either 50 or 200 mm Hg, an intraneural edema developed.(ABSTRACT TRUNCATED AT 250 WORDS)